LIVERDISEASESANDITS

ANESTHETICIMPLICATIONS
ANATOMY
MICROSTRUCTURE AND HISTOLOGY
 HEPATIC BLOOD SUPPLY
- 25% to 30% of CO

Dual supply

Portal V (75%) - 50-60% of oxygen supply

Hepatic A (25%) - 40-55% of oxygen supply

HEPATIC BLOOD FLOW
CONTROL OF LIVER BLOOD FLOW

1) 1) HEPATIC ARTERIAL BUFFER

RESPONSE
mostimportantintrinsicmechanism
changesinportalvenousflowcausereciprocal
changesinhepaticarterialflow
mechanisminvolvesthesynthesisandwashoutof
adenosine(i.e.,avasodilator)fromperiportal
regions
2) AUTOREGULATION

Mechanisminvolvesmyogenic responsesof
vascularsmoothmuscletostretch
Onlyinpostprandialstate

3) METABOLIC CONTROL
-Decrease oxygen tension or ph of portal
venous blood increase hepatic arterial flow
whereas postprandial hyperosmolarity
increase both hepatic and portal flow
 B.EXTRINSIC REGULATION
1.NEURAL CONTROL
-Fibers of the vagus, phrenic, and splanchnic nerves (postganglionic
sympathetic fibers from T6 through T11)
-When sympathetic tone : splanchnic reservoir volume increases.
-Vagal stimulation : alters the tone of the presinusoidal sphincters
-the net effect is a redistribution of intrahepatic blood flow without
changing total hepatic blood flow.
2.HUMORAL CONTROL
- hepatic arterial bed has 1-, 2-, and 2-adrenergic receptors
- portal vein has only -receptors
Glucagon induces relaxation of hepatic arterial smooth muscle.
angiotensin II constricts the hepatic arterial and portal venous beds.
Vasopressin elevates splanchnic arterial resistance, but it lowers
portal venous resistance.
SPECTRUM OF LIVER DISEASE
PARENCHYMAL
- Acute infectiousornoninfectious
ChronicHepatitis alcohol,autoimmune,drugs,
inherited(wilson,alpha1antitrypsin),NASH,viral
HepaticCirrhosis(+portalhypertension)
CHOLESTATIC
Intrahepatic
viralhepatitis
druginduced
Extrahepatic (Obstructivejaundice)
Calculi,stricture,growth.
 CIRRHOSISOFLIVER
Achronicprogressivedisease
Extensivedegeneration&destructiontothe
liverparenchymal cells
Cellnecrosis scartissue nodular
structure impedesbloodflow hypoxia
 Causes
Chronicviralhepatitis
Metabolic:hemochromatosis,Wilsondis,
alfa1antitrypsin,NASH
Prolongedcholestasis (primarybiliary
cirrhosis,primarysclerosing cholangitis)
Autoimmunediseases(autoimmune
hepatitis)
Drugsandtoxins
Alcohol
 Pathophysiology
Alcoholiccirrhosis accumulationoffatand
scarformationinthelivercells
Postnecrotic cirrhosis broadbandsofscar
tissueresultedfromviral,toxic,or
autoimmunehepatitis
Biliary cirrhosis diffusefibrosiswithjaundice
fromchronicbiliary obstruction
Cardiaccirrhosis fromlongstandingright
sidedheartfailure
 ClinicalManifestations
Early
GIdisturbances,dullpaininRUQ/epigastrium,
fever,malaise,enlargementofliver&spleen
Late
Jaundice,skinlesions(spiderangiomas,palmar
erythema),hematologicproblems,endocrine
disturbances,peripheralneuropathy
 Complications
1. PortalHtn
2. Oesophagogastric varices
3. Ascites
4. Anemia&coagulopathy
5. SBP(spontaneousbacterialperitonitis)
6. Cardiomyopathy
7. Arterialhypoxemia&Hepatopulmonary syndrome
8. Hepatorenal syndrome
9. Hypoglycemia
10. Duodenalulcer
11. Gallstones
12. Hepaticencephalopathy
13. PrimaryHCC
 Pathophysiology ofEndStageLiver
Disease
Predominantpathophysiological manifestationof
liverdiseaseisportalhypertension.
Normalportalpressuresareusuallyintherange
of512mmHg.
Portalhypertensionisgenerallydefinedwhen
any2ofthefollowing3criteriaaremet:
splenomegaly,ascites orbleedingesophageal
varices.
Portalpressuresatthistimeareusually>20
mmHg
 Varices
Duetoportalhypertension
Varicositiesdevelopwherecollateral&
systemiccirculationscommunicate
esophageal&gastricvarices,caputmedusae,
&hemorrhoids
mostcommongastroesophageal varices
Painlessmassivehaematemesis withor
withoutmelena &otherfeaturesofPH.
Endoscopy bestforevaluation
Collaterals
SITES:
1. Oesophagus

2. Gastric

3. Colorectal

4. Portalhypertensive
gastropathy
 STANDARDTREATMENTOFPORTAL
HYPERTENSION
1. Preprimaryprophylaxis EGD,notreatmentforPH,treatcause
ofcirrhosis.
2. Primaryprophylaxis nonselectivebblockers(propranolol,
nadolol)areaseffectiveasEndoscopicvariceal ligation(EVL)
dependinguponrisk
3. Controllingacutevariceal hemorrhageSafevasoactive drugsare
startedassoonaspossible,priortodiagnosticendoscopy.EVLis
theprocedureofchoiceifsourceconfirmed,Sclerotherapy
secondline.TIPSrecommendedwheneverythingfails
4. Secondaryprophylaxis ifTIPSperformedconsiderfortransplant.
IfTIPSnotperformedcombinationofpharmacological(NSBB
aloneorNSBB+ISMN)plusEVLisassociatedwithlower
rebleeding ratesthaneithertherapyalone
 Ascites
Accumulationofserousfluidinperitoneum

OVERFLOW MODEL excessive renal

retention of sodium intravascular volume
to expand, causing
(1) plasma oncotic pressure decreases, with the
liver unable to produce sufficient
(2) portal hydrostatic pressure increases
The combination of low oncotic pressure
and portal hypertension accelerates the
formation of edema and ascites.

UNDERFILL MODEL cirrhosis causes the

effective plasma volume to decrease, which
activates homeostatic mechanisms to retain
sodium and water.
 Tenseascites maydecreasefunctionalresidual
capacity(FRC),adverselyaffectpulmonarygas
exchangeandincreaseriskofaspiration.
Hydrothoraxorpleuraleffusionsmayproduce
atelectasis.
Secondaryhyperaldosteronism maymanifestas
hypokalemic metabolicalkalosis.
Thereisintraandextrapulmonaryshunting,
elevatedmixedvenousoxygensaturation(SvO2),
alteredlactatemetabolism.
Treatment diagnosticparacentesis,saltrestriction
to2000mg/day,diuretics(furosemide or
spironolactone ),Largevolumeparacentesis,TIPS
 COAGULOPATHY
AllcoagulationfactorsexceptforVIIIaremarkedlyreducedinpatients
withliverdisease
CLDpatientshavethrombocytopeniaduetosplenomegaly and
decreasedthrombopoeitin
AntithrombinIII(ATIII)levelsfallduetoreducedsynthesisand/or
increasedconsumptionduetofibrinolysis
Hemostatic changesassociatedwithsurgicalbleedingare
1. thrombocytopenia,
2. plateletfunctiondefects,
3. inhibitionofplateletaggregationandadhesionbynitricoxideand
prostacyclin,
4. decreasedlevelsofcoagulationfactors:II,V,VII,IX,X,XI,quantitative
andqualitativeabnormalitiesoffibrinogen,
5. lowlevelsof2antiplasmin,FactorXIIIandthrombinactivatable
fibrinolysis inhibitor,andelevatedtPA.
 Hemostatic changesassociatedwiththrombosis:
1. ElevatedvWF,decreasedlevelsofADAMTS13(a
vWF cleavingprotease),
2. Decreasedlevelsofanticoagulants:ATIII,Protein
CandS,2macroglobulin,elevatedlevelsof
heparincofactorII,elevatedVIII,decreasedlevels
ofplasminogen,normalor increasedPAI1.
3. Hypercoagulability canoccurinpatientswithliver
disease,especiallythosewithcholestatic disease.
 Portopulmonary hypertension(POPH)
Pulmonaryhypertensionsyndromewithvascularobstruction
andincreasedresistancetopulmonaryarterialflow
Itoccursduetopulmonaryendothelial/smoothmuscle
proliferation,vasoconstrictionandinsituthrombosis.
ThedevelopmentofPOPHhasnotbeendemonstratedto
correlatewiththeseverityofliverdisease
ThediagnosticcriteriaforPOPHincludeameanpulmonary
arterypressure(mPAP)greaterthan25mmHgatrestanda
pulmonaryvascularresistance(PVR)of>240dynes.s.cm.
Abettermeasureisatranspulmonary gradient>12mmHg
(mPAPPAOP)asthisreflectstheobstructiontoflow(PVR)
 Femalegenderandautoimmunehepatitishave
beenreportedtoberiskfactors.
Incasesconfirmedbyrightsidedheart
catheterization,treatmentwithepoprostenol or
bosentan mayreducepulmonaryhypertension
andtherebyfacilitatelivertransplantation;
Livertransplantationiscontraindicatedin
patientswithmoderatetoseverepulmonary
hypertension(meanpulmonarypressure>35
mmHg).
 Hepatopulmonary syndrome(HPS)
Characterizedbyarterialhypoxemia
causedbyintrapulmonaryvascular
dilatations.
Theclinicaltriadof
1)portalhypertension;2)hypoxemia;
and3)pulmonaryvasculardilatations
 EuropeanRespiratorySociety(ERS)/European
AssociationforStudyoftheLiver(EASL)TaskForcehave
certainsetdiagnosticcriteriaforhepatopulmonary
syndrome(HPS).
Theseinclude:
Diagnosisofliverdisease,
AnAaoxygengradient>15mmHg,
Pulmonaryvasculardilatationdocumentedby
positive"delayed,contrastenhanced
echocardiographywithleftheart,
Detectionofmicrobubbles for>4cardiaccyclesafter
rightheartopacification ofmicrobubbles
Brainuptake>6%following99mTcmacroaggregated
albumin(MAA)lungperfusionscanning
 TREATMENT
Medicaltherapyhasbeendisappointing
Experimentally,ivmethylene blue,oralgarlicpowder,andoral
norfloxacin mayimproveoxygenationbyinhibitingnitricoxide
inducedvasodilation
Pentoxifylline maypreventhepatopulmonary syndromeby
inhibitingproductionoftumornecrosisfactor.
Longtermoxygentherapyisrecommendedforseverely
hypoxemicpatients
Thesyndromemayreversewithlivertransplantation,although
postoperativemortalityisincreasedinpatientswitha
preoperativearterialoxygentension<50mmHgorwith
substantialintrapulmonaryshunting.
TIPSmayprovidepalliationinpatientswithhepatopulmonary
syndromeawaitingtransplantation.
 Hepatorenal syndrome
Prerenalacutekidneyinjurythatoccursin
decompensated cirrhosis.
Thesyndromeisclassifiedintotwotypes:
Type1ischaracterizedbyadoublingoftheserum
creatinine leveltogreaterthan2.5mg/dlinless
than2weeks
Type2ischaracterizedbyastableorslower
progressivecourseofrenalfailure
 TheInternationalAscites ClubhassuggestedFIVE
majorcriteriatoconfirmthediagnosisofHRS:
(1)chronicoracuteliverdiseasewithadvancedhepatic
failureandportalhypertension;
(2)alowGFRasassessedbyserumcreatinine >1.5
mg/dL orcreatinine clearancebelow40mL/min;
(3)absenceofshock,ongoingbacterialinfection,fluid
losses,ortreatmentwithnephrotoxic drugs;
(4)nosustainedimprovementinrenalfunctionafteroral
diureticwithdrawalandplasmavolumeexpansion;and
(5)lessthan500mg/dayproteinuria withno
ultrasonographic evidenceofparenchymal renal
diseaseorurinaryobstruction
 MANAGEMENT
IVinfusionofalbumin+vasoconstrictorregimensfor714
days:
1. IVvasopressinorornipressin (ischemics/e);
2. IVornipressin plusdopamine;
3. IVterlipressin (preferredagent);
4. IVnorepinephrine;
5. oralmidodrine,anadrenergicdrug,plusthesomatostatin
analogoctreotide,s/coriv.
MARS(molecularadsorbentsrecirculating system ),a
modifieddialysismethodthatselectivelyremovesalbumin
boundsubstances.I
TIPS
Livertransplantationisthetreatmentofchoice.
 Spontaneousbacterialperitonitis
Consistsoffever,leukocytosis,abdominalpain,
anddecreasedbowelsounds
gutwallpermeabilitygrowthofbacteriain
peritonealfluid
Associatedmacrophagefunc on
Riskfactors lowproteininascitic fluid,variceal
bleeding
AntibioticprophylaxisinPtswithGIhaemorrhage
isrecommended.
Highmortality(2050%)
 HepaticEncephalopathy
Pathophysiologic phenomenathat
contributetothesyndromeinclude
(1)hepatobiliary dysfunction,
(2)decreasedhepaticbloodflow,
and
(3)extrahepatic diversionofportal
venousflowthroughcollateral
vessels

Euphoria,irritability,confusion,
slurredspeech,slow&deep
respiration,hyperactivereflexes,
positiveBabinskis reflex

Asterixis,fetorhepaticus,deep
coma
 FactorsThatMayPrecipitateHepatic
Encephalopathy
Excessivedietaryprotein
Constipation Increasedammonia
Gastrointestinalbleeding production
Infection
Azotemia

Diarrhea andvomiting Dehydrationwithelectrolyteandacidbase

Diuretictherapy imbalance,increasedammoniageneration,and
Paracentesis decreasedhepaticperfusion

Hypoxia
Hypotension
Anemia Adverseeffectonliverandbrainfunction
Hypoglycemia

Sedatives/hypnoticsActionattheGABAA/benzodiazepinereceptorcomplex

CreationofportalsystemicshuntReducedhepaticmetabolism
 MANAGEMENT
Dietaryproteinwithheldorlimitedto6080g/d;vegetableprotein
better
ControlGIbleedandpurgebloodout.120mL ofmagnesiumcitrate
orallyorNGtube34hrlyuntilthestoolisfreeofgrossblood,orby
administrationoflactulose (twoorthreesoftstoolsperday)
Oralantibiotic;nonabsorbable agentrifaximin,400mgorallythree
timesdaily,ispreferred.Otheragentsmetroinidazole orneomycin
Flumazenil iseffectiveinabout30%ofpatientswithseverehepatic
encephalopathy,butthedrugisshortactingrequiringiv
administration.
Branchedchainaminoacidsunnecessaryexceptpatientswhoare
intolerantofstandardproteinsupplements.
Treatmentwithacarbose (analphaglucosidase inhibitor)andL
carnitine (anessentialfactorinthemitochrondrial transportoflong
chainfattyacids)isunderstudy
connection.lww.com/Products/morton/Ch41.asp
PREOPERATIVE ASSESSMENT

OBJECTIVES
1. Assessthetypeanddegreeofliverdysfunction.
2.Typeofsurgery
3. Assesseffectonothersystem.
4. Toensure postoperativefacilities(Highriskpatient).
PREOPERATIVE ASSESSMENT
HISTORY
-Dyspnoea,syncope,bleeding,delerium,effort
tolerance

CLINICAL EXAMINATION
- Bloodpressure,pulse,oxygenation,bruising,
ascites,orientation,jaundice

INVESTIGATIONS
 PREOPERATIVE INVESTIGATIONS
A)TO ASSESS GENERAL CONDITION OF PATIENT

1)Haematological 3)Metabolic
Hb Serumproteins
TLC,DLC Serumglucose
PlateletCount Electrolyte
Clottingfactors Urea/Creatinine
(PT,PTTk)
2)Cardiorespiratory
ChestXray
ECG
Pulmonary.fn.tests
Bloodgases
Echocardiography
B) TO KNOW THE PATTERN OF DISEASE

S.Bilirubin
SGOT,SGPT90%predictive
Alk.phosphatase
SingleMarker
GlutathioneStransferase druginduced
Glutamyltranspeptidase alcohol/druginduced
C) TO JUDGE THE SYNTHETIC ABILITY OF
LIVER
Serum albumin < 25 gm% - severe damage
Albumin/globulin ratio reversed.
Prothrombin time > 15 sec. Over control
INR - > 1.3

C) OTHER TESTS (DONE ONLY FOR MAJOR

SURGERY)
- liver biopsy
- screening for hepatitis
- feto protein Hepatocellular Carcinoma
- Antinuclear antibodies prim. biliary cirrhosis
- Copper & Ceruloplasmin level Wilson's disease
ferritin and transferritin Haemochromatosis
 CardiacassessmentofEndStageLiver
Disease(ESLD)patients
Maydevelopcirrhoticcardiomyopathy
IncreasedCOandcompromisedventricular
responsetostressleadstocardiacdepressionand
repolarization abnormalities
Lowsystemicvascularresistanceandbradycardia
IncreaseQTinterval,electricalandmechanical
dyschrony ,chronotropic incompetence
CandevelopCADifcardiacriskfactorspresent
Leftventricularoutflowtractobstruction(LVOTO)
 ROLEOFECHO
Preop echo
1. Ventricularfunction,size
2. Valvular function
3. Pulmonaryarterypressure
4. ExcludeanyLVOTOorpericardialeffusion
5. Pulmonaryarterysystolicpressure
calculation
 TEEand/orpulmonaryarterycatheterization
maybeusedintraoperatively toallowforreal
timehemodynamicmonitoringandvolume
management.
StresstestingofESLDpatientscanbedoneto
detectCAD.
Coronaryangiographyisthegoldstandardfor
detectingCAD
Rt heartcatheterizationroletomeasure
PAP,PCWPandTPG
GRADING OF SEVERITY OF DISEASE

MildHepaticdysfunction
Cl.History+evidenceofliverpathology
normalplasmaalbumin,butenzymes

ModerateHepaticdysfunction
Limitedimpairmentofsyntheticfunction
PTnot>25sec.abovenormal
Plasmaalbuminatleast3gm%.

Severehepaticdysfunction
Moreimpairmentofsyntheticfunction.
 SurgicalRisk.
Electivesurgeryiscontraindicatedwhenthepatient
hasacuteviralhepatitis,alcoholichepatitis,
fulminant hepaticfailure,severechronichepatitis,
isaChildPughCpatientorhasothermanifestations
ofendstageliverdisease.

Tworiskstratificationschemesdevelopedtoassess
theperioperative riskofpatientswithcirrhosis:
1. ModifiedChild Turcotte PughScoringSystem
2.TheModelofEndStageLiverDisease(MELD)score
ModifiedChild Turcotte PughScoringSystem

1 2 3
S.Bilirubin <2gm% 2 3gm% >3gm%

S.albumin >35gm% 2.835g% <2.8gm%

Ascites None slightmoderate tense

Encephalopathy None GradeI&II GradeIII&IV

Prothrombintime

Secprolonged <4 4 6 >6

INR <1.7 1.7 - 2.3 >2.3

ModifiedChild Turcotte PughScoringSystem

CLASSES SCORE MORTALITY

A 56 10%

B 79 31%

C 1015 76%
MELD

Objectiveassessmentinpredicting3monthmortality
Primarilyusedtoselectpatientsforlivertransplant
0.38Xln (bilirubin mg/dl)+1.12Xln (INR)+0.96
ln (creatinine mg/dl)+0.64

Bestoutcomes:MELDscore<14.

ForpatientswithaMELDscoreof1524
Clinicaljudgment
Furtherdiscussionwiththefamilyandthepatient
Preoperativeapproach:PatientwithKnown/
Suspectedliverdisease
PERIOPERATIVE MANAGEMENT
PREOPERATIVE PREPARATION
(1) ChildsGroup
A ElectiveSurgeryrecommended
B acceptableaftercorrection
C onlyforemergency

(2)Assesshydrationstatus.

(3)CorrectAnemia/Coagulation/hypoalbuminemia

(4) Arrangeappropriateblood/bloodproducts.

(5) Inform postoperativecomplications

 PREMEDICATION

Ifneuro.statusnormalanxiolytic (oral)
oralH2antagonist
Vit.K(Obst.J) 10mgBDX3day
IfBilirubin >8mg%
Mannitol 100mlof20%2hrspreop
ANAESTHETIC MANAGEMENT
GENERALCONSIDERATIONS
Minimizephysiologicalinsulttoliver&kidney
MaintainO2supply demandrelationshipinliver.
Adequatepulmonaryventilationandcvs fn.
Maintainrenalperfusion
AvoidHypotension,hypoproteinemia &hypoxiaMeticulous
fluidbalance

Chooseappropriateanaesthetic agent
Metabolismofdrugs+EffectonHBF
General anaesthesia
Induction agent

Thiopentone / propofol

Given in slow tirated dose

Avoid hypotension

Avoid sympathetic stimulation

Propofol :
Highly lipid soluble

High extraction ratio

However kinetic profile similar to normal patients

Thiopentone :
Low extraction ratio

Elimination half life unaltered secondary to increased Vd

Musclerelaxants
DecreasedS.Alb Increasedfreedrugconcentration
Drugswithhepaticclearanceavoided

Vecuronium
Rocuronium
Pancuronium
Mivacurium (infusionavoided)

Atracurium/Cis atracurium Nonspecificesterhydrolysis

Succinylcholine ForRSI
Afterscreeningfortheusualcontraindications
Prolongedimmobility
Criticalillness
Hyperkalemia

Severeliverdysfunction decreasecholinesteraseactivity
Mayprolongtheeffectofsuccinylcholine somewhat
Rarelycausesaclinicalproblem.
Morphine
Reducedmetabolism
Prolongedeliminationhalflife
Inc.Bioavailability
Inc.SedativeandRespiratorydepressanteffects
Administrationintervalshouldbeincreased1.5 to2foldinthesepatients

Meperidine
50%reductioninclearance
Doublingofthehalflife
Inaddition,clearanceofnormeperidine isreduced
Patientswithsevereliverdiseasemayexperienceneurotoxicity
Fentanyl andSufentanil
Nosignificantchangeinpharmacokinetics

Repeatedadministrationorcontinuousinfusions,accumulationmayoccur
andleadtoprolongedeffects

Alfentanil
Showsdecreaseinplasmaclearance

Halflifeisalmostdoubledinpatientswithcirrhosis

Remifentanil
Eliminationisunalteredinpatientswithsevereliverdisease
SpasmOfSphincterOfOddi

Opioidscancausespasmofsphincterofoddi
Increasecommonbileductpressures

Morewithmorphine,fentanyl,meperidine

Avoidedifintraoperative cholangiogram tobedone

Treatment Opioid antagonists(naloxone)

Smoothms.relaxant(nitroglycerine)

Glucagon
Sedatives
Midazolam :
Reducedproteinbindingandincreasedfreefractions
Reducedclearanceinpatientswithendstageliverdisease
Producesprolongedeliminationhalflives
Enhancedsedativeeffectespeciallyaftermultipledosesorprolonged
infusions

Dexmedetomidine
Primarilymetabolizedintheliverwithminimalrenalclearance.
Patientswithhepaticfailureofvaryingseverityhave
Decreasedclearance
Prolongedhalflives
Lowerbispectral indexvalues
Hencedoseadjustmentsindicated
Voltaile Anesthetics

Useful&welltolerated
Canbeentirelyeliminated

Sevoflurane :Mosteffectiveinmaintaining
HBF
HepaticO2delivery

Isoflurane /:Verygoodmaintainance of
Desflurane HBF
HepaticO2delivery
O2deliverytoconsumptionratio
 Halothane
Halothane(avoided)
Detrimentalreductionsin
Hepaticoxygendelivery
HBFbyalterationsin
Cardiacoutput
MAP

Halothanehepatitis(rare)
 ClinicalFeaturesofHalothane
Hepatitis
MildFormFulminant Form
Incidence,1:5Incidence,1:10,000
RepeatexposureMultipleexposures
not
MildelevationofMarkedelevationof,
ALT,ASTALT,AST,bilirubin,
FocalnecrosisMassivenecrosis
SelflimitedMortalityrate,50%
Antibodiespresent
Xenon:
Consideredtobeanidealinhaledanesthetic

Nonexplosiveandnonflammable

Rapidinductionandrecoveryprofiles

Cardiacstability

ItdoesnotalterHABF

Doesnotaltertheresultsofliverfunctiontests

Animalsexposedtoxenon:Higherhepaticvenousoxygencontentlevels

Secondarytoapossiblereductionofplasmacatecholaminelevels

Subsequentreducedhepaticmetabolism

Xenonmayprovetobeanidealanestheticrelativetohepaticperfusion.
 Intraoperative considerations
IVaccessusinglargeboreperipheralcathetersaswellascentral
venousaccesscatheters.
RSIintenseascites ptriskofaspiration
Preventingcirculatorycllapse byadministrationofIVcolloidsolutions
becauseintravascularvolumereequilibriumoccurs6to8hrsafter
removaloflargervolumesofascitic fluid.
Largevolumesofcolloids/crystalloidsmaybegivenwithinafew
minuteswiththeassistanceofcommerciallyavailablerapidinfusion
devices.
RedcellsalvageshouldbefacilitatedwithuseofCellsavers
with/withoutleukocytefilters.
Bloodadministrationmaybeassociatedwithhyperkalemia and
hypocalcemia.
 Bleedingduringliversurgerycouldbeeither
surgical,duetopreviousoracquiredcoagulation
disturbances,orboth.
ThepreoperativeINRhasnopredictivevalue
FFProledebatable
Intraoperative hemostasis panelsconsistingofINR,
fibrinogenandplateletcount,andplateletfunction
assaysforbothplateletcountandfunction.
 ROLEOFTHROMBOELASTOGRAPH
Thromboelastograph (TEG) usefulintraoperative testfor
coagulation
Neteffectofproandanticoagulantandproandanti
fibrinolytic factorsandtheresultingclottensilestrength.
Rate,strengthofclotformationandclot
stability/fibrinolysis.
Fordetectingintraoperative hypercoagubility.
TEGfacilitatespecificgoaldirectedtherapy.
Fibrinolysis diagnosedontheTEGcausingclinically
significantmicrovascular ooze,small dosesofepsilon
aminocaproic acid(EACA)ortranexamic acid(TA)are
suitableantifibrinolytics.
FactorVIIhasbeenusedtocontrolmassivebleeding
duringliversurgery;
IntraOperativeMonitoring

Routine
NIBPECG
EtCO2SPO2
UrineoutputN/msmonitoring

Longerandextensivesurgeries
CVP
ABG
Invasivebloodpressuremonitoring
S.Electrolyte,Bloodsugars
TEG
POSTOPERATIVE MANAGEMENT

1)MinorSurgeryormildmod.liverdysfn.
N/msblockreversedExtubate
2)Majorsurgery/severeliverdysfn.
ContinueIPPVinP.op.period
Fluid&Electrolyteimbalancecorrected
CVSstabilityachieved
Hypothermiacorrected
UrineOutput1ml/kg/hr
3) Adequateanalgesia(Smalldoses)
4) Blood/bloodproductreplaced.
 Postoperativepainrelief
Thoracicepiduralanalgesiaprovidesexcellentanalgesiafor
liverresectionsbutrestrictedduetocoagulationdefects
ThecatheterisusuallyinsertedattheT6T9space.
Ropivacaine orbupivacaine arecommonlocalanesthetics
usedwithorwithouttheadditionofsmallamountsofopioids
suchasfentanyl,sufentanil,hydromorphone ormorphine.
Italsoreducesthegastrointestinalparalysiscomparedwith
systemicopoids
NSAIDSriskofGIbleeding,plateletdysfunctionand
nephrotoxicity ;avoided.
Paracetamol issometimesused
Fentanyl PCAisgenerallywelltolerated
MorphinePCAcanalsobeusedbutalowerbolusdosemay
beneeded,againtoavoidaccumulation.
 POSTOPERATIVE JAUNDICE

Incidence < 1%
- Cause - Overproduction or under
excretion
of bilirubin
- direct hepatocellular injury
- extrahepatic obstruction
- Mild < 4mg/dl
- Severe > 4mg/dl
CausesOfPostoperativeLiverDysfunction
 Agent Hepatocellular Steatosis Cholestasis
Acetaminophen *
Alcohol *
Amiodarone *
Aspirin * *
Amoxiclav *
Isoniazid *
Ketoconazole *
Methotrexate * *
Phenytoin *
Anabolicsteroids *
OCP *
Sulfonamides *
Valproic acid *
TPN *
Tetracycline * *
 Transjugular Intrahepatic Portosystemic Shunt
Percutaneously createdintrahepatic connectionoftheportaland
systemiccirculations

1.StentispassedthroughtheIJVoverawireintothehepaticvein

2.DilatedEVareapparent.Thewireandstentarethenadvancedintotheportalvein

3.BloodcanpassthroughthePVintotheHVandbypassanddecompressdilatedesophagealveins
Typicallyusedinpatientswithendstageliverdisease
Todecreaseportalpressure
Attenuatethecomplications
Varicealbleeding

Refractoryascites

Complications
Encephalopathy
Stentstenosisandocclusion
 Hepaticresection

Preoperativeconsiderations
Involveriskassessment:MELDclassification.

Severethrombocytopeniaorlargevarices:Majorperioperative risk

Fluidmanagement:Controversial.
Liberaluse:Goalofincreasingintravascularvolumeasabuffer.

Lowcentralvenouspressure:MinimizebloodlossfromMajorveins

Intravenousfluids
Supplementedsodiumorpotassiumphosphate
Hepaticcryotherapy
Treatnonresectable malignanthepatictumors
Involvesusageofsubzerotemperature
MultiplelumenprobespositionedunderUSGguidance
Heatconservationinstitutedduringtheprocedure
Withcontinualmonitoringofcoretemperature.
Cryoshock syndrome:
Postoperative
Pulmonary
Renal
Coagulationproblems
Livertransplantation:Advancesand
perioperative care
 LIVERTRANSPLANT
INDICATIONSCONTRAINDICATIONS
HEPATITISSEPSIS
ALDCARDIOPULMONARYDISEASE
HEMOCHROMATOSISEXTRAHEPATICMALIGNANCY
PBCAIDS
PSCANYSUBSTANCEABUSE
CFUNFAVPSHYCHOSOCIAL
WILSONCIRCUMSTANCE
AMYLOIDOSIS
MALIGNANCY
BUDDCHIARI
 STAGES
Preanhepatic fromstartofsurgery
toclampingofhepaticartery
Anhepatic fromclampingto
reperfusionofnewliver
Postanhepaticfromreperfusionto
endofcase
 Orderofreconstruction
Standardmethodsuprahepatic ivc followedby
infrahepatic ivc anastomosis PVanastomosis arterial
reconstruction biliary drainage
Piggybackmethod onlyoneivc anastomosis

Testclampmaneuver
Usedinstandardmethodtoassessresilienceof
circulatorysystem
Suprahepatic ivc clamped arterialpressure,CO
decrease
Ifexcessivecirculatorydepressionproceedingsdelayed
,reassessvolumestatus,cardiacperformance
,metabolicstate.
Venovenous bypassifstillcirculatorydepression
 Intraoperative Monitoringand
Management
Haemodynamic monitoringstandard
cardiovascularmonitors(electrocardiogram,
pulseoximetry,invasiveandnoninvasiveblood
pressure)
AdditionallyrequiresCOmonitoring
Pulmonaryarterycatheter(PAC)isthegold
standardusedinhaemodynamic monitoring
Monitoringofcentralvenousoxygensaturation
andmixedvenousoxygensaturationduringliver
transplantationisoflittlevalue
Hemodynamicmanagement
Duringthedifferentstagesoflivertransplantation,
i.e.preanhepatic phase,anhepatic phaseand
neohepatic phase,therearerapidfluidshiftsdueto
bloodloss,inferiorvenacavaclampingand
reperfusion.
Decreasingcentralvenouspressure(CVP)eitherby
phlebotomyoravoidingplasmatransfusionduring
thepreanhepatic phasehaveshowntoreducered
celltransfusions
 Vasopressinisoftenaddedintraoperatively to
maintainthesystemicvascularresistance.
Vasopressinreducesportalbloodflowby
selectivesplanchnic vasoconstrictionandhence
maybeusefulinreducingtheintraoperative
bloodloss.
Methylene blueatadoseof0.5mg/kgbody
weightover10minrescuetotreathypotension
duetovasopressorresistantvasoplegic shock.
Phenylephrine isoftenusedtotideoveracute
hypotensive episodes
 Fluidmanagement
Livertransplantsurgerymassivefluidshiftsboth
fromintravascularvolumedepletionandlarge
surgicalbloodloss.
Albumincanbeusedasptsarehypoalbuminaemic
andhypovolaemic ;costfactorlimitsituse
CrystalloidsusedependsontheirpH,electrolyte
composition,osmolarity andmetabolism
 Noidealcrystalloidsolution
0.9%NScauseshyperchloremic acidosiswhilethe
lactateinRingersLactate(RL)requiresliver
metabolismforitselimination.
RLisahypotonicsolutionandmayincreasethe
intracellularfluid.
Plasmalyte hasapHnearnormal,electrolyteand
osmolarity similartoplasmaandacetate,whichis
metabolised extrahepatically tobicarbonate,but
itisproinflammatory andpotentiallycardiotoxic.
 Coagulationmonitors
PTandAPTTlimitedrole
Thromboelastogram (TEG),rotationalthromboelastometry
(ROTEM)andSonoclot provideadetailedassessment
Bloodcomponentmanagement
Preanhepatic phaseisassociatedwithbloodloss
Theaimatthisstageistoavoidlargevolumeoftransfusion
anddilutional coagulopathy
Antifibrinolytics areusedinthelivertransplantationto
preventthehyperfibrinolytic stateduringtheanhepatic and
neohepatic phases
Theneohepatic phaseisassociatedwithamultifactorial
coagulopathy ofhyperfibrinolysis,dilutional coagulopathy,
heparinlikeeffect,plateletdysfunction,hypothermiaand
hypocalcaemia
Ischemiareperfusioninjury
Ischemiareperfusioninjury(IRI)isassociatedwith
primarygraftdysfunctionanddelayedgraft
function
Nacetylcysteine (NAC)isbeingusedinliver
transplantationpatientstopreventrenalfailureand
IRIofthenewliver.NAC,inadditiontoitsdirect
antioxidantproperty,replenishesglutathioneand
actsasafreeradicalscavenger.
Inhalationalanaesthetics,especiallysevoflurane,
havebeenshowntoofferprotectionagainstIRIin
themyocardiumincardiacpatients
 Earlyextubation inselectedpatientsimprovesearly
graftfunctionandreducedurationofstayinthe
IntensiveCareUnitandnosocomial infections
Selectionofpatientsforearlyextubation depends
ondurationofthesurgery,amountofbloodand
productstransfused,patients'preoperativestatus
(MELDscore),ischaemia timeandstatusofthe
graft.
Asafeoperatingroomextubation afterliver
transplantation(SORELT)predictionrulemaybe
usedtoselectpatientsforearlyextubation,but
requiresvalidation
 CONCLUSION
Patientswithliverdiseaseareatincreasedrisk
forbothperioperative morbidityand
mortality.
Themultisystemimpactofliverfailuremeans
assessmentandmanagementofthese
patientsoftenrequiresmultidisciplinary
discussionandcriticalcareadmissionto
optimise outcome
THANKYOU
 ROLEOFTHROMBOELASTOGRAPH
ParameterInterpretationPreferredtherapyfor
abnormalvalues
RR isthetimeoflatencyFFP
placedintheTEGanalyzer
untilinitialfibrinformation
Thevaluemeasuresrapidity
offibrinbuildupandcrosslinkingCryoprecipitate
KK timeisameasureofthe
rapiditytoreachcertainlevelFFP
ofclotstrength.

MAMA,orMaximumAmplitude,
directfunctionofthemaximumPlatelets
dynamicpropertiesoffibrin
andplateletbondingandrepresents
theultimatestrengthoffibrinclot.